Concept of source-load

The concept of source-load or source-sink is not talked about very much in books – but is a very elegant explanation of how conduction propagation occurs in cardiac tissue and how this leads to arrhythmia. ( For reference Prof Antonio Zaza gives a very nice description of this on the ESC learning platform.)

This article is my simple take on it as it helps to understand certain arrhythmia phenomena

In the section on re-entry we saw how a re-entrant circuit is formed. Anatomically, basically its a strip or zone of conducting myocardium connected at the ends and separated by an obstruction.

How does actual cellular conduction occur cardiac myocites?. First, the initiating cell must depolarize – this means opening of sodium channels – and flooding the cell with sodium ions. The cell has gap junctions – specialized connections with adjacent myocadial cells and these gap junctions permit rapid conductance of ions to the adjacent cell. Therefore the sodium ions get to travel to the adjacent cell rapidly. This increases the membrane potential in that cell sufficiently that it then depolarizes too. If that cell is connected to other cells, the sodium ions spread through the gap junctions to those cells, repeating the process and the impulse continues to propagate.

Lets look at a diagram :

Source load concept in myocardial signal conduction -mechanism at channel level
During an action potential, opening of Na channels - leads to flooding of the cell with Na ions. These ions then travel to adjacent cells via gap junctions and depolarize the receiving cell too. The process keeps on repeating and the impulse propagates along connected cells.

In reality, one cell is connected to many cells. Given that a single cell has only so many sodium ions, if the cell is connected many cells, the ions get distributed among the cellsĀ  – in other words, the subsequent cells get a lesser amount of ions. If the amount of ions are sufficient, the cell may depolarize but at times the amount of ions may not be adequate to raise the membrane potential for depolarization.

The initiating cell/s are called the source and the receiving cells are called the load. It is similar to electrical terminology – where if the current load is too much the source will fail to power the load.

In real life each cell has a safety factor to ensure that many cells are depolarized so that impulse propagation is maintained. Some cells have huge amounts of sodium ion currents – like the Purkinje cells – as they need to supply a large number of cells. (i.e. have a big load). So Purkinje cells are said to have a large safety factor.

Source load concept in myocardial signal conduction -mechanism at channel level
A single cell connects to two cells - and the sodium ions from the initial cell gets distributed to both cells - which means the receiving cell may not get enough ions to initiate a depolarization on its own membrane.

If more and more cells are connected in a given pathway, its logical that you need more ions at the beginning to drive the depolarization process. The next diagram shows a strip of myocardial cells bordered by scar tissue.

In very simple form, there is an asymmetry of the tissue segment with the left hand side thin and narrow and the right had side broad. The thin part has less cells to recruit for depolarization and therefore an impulse arriving from the left side will face an uphill (difficult) task of providing enough ions to pass the depolarization to the right side as more cells are there to dilute the incoming ion supply.

In contrast, any impulse coming from the right side would be loaded with ions from many cells and by the time it reaches the thin segment, it would be more than enough to propagate the impulse to the left side.

This is how a thin segment of a scar can lead to a unidirectional block.

If you remember, a unidirectional block is one requirement for initiating re-entry !

Source load concept in myocardial signal conduction - mechanism of unidirectional conduction in a asymmetric scar channel
The asymmetric distribution of myocardial cells bordered by scar tissue - leads to a source -load mismatch in one direction causing a unidirectional block (see text)

This concept also explains why concealed accessory pathways are common (they generate orthordomic AVRT) and even in manifest WPW, orthodromic AVRT is common. The ventricular myocardium is a huge source compared to the atrial myocardium – and during tachycardia when the whole ventricle is depolarized, conduction preferentially happens from atrium to ventricle more than the other direction.This concept also explains why despite a delta wave (which indicates forward conduction from the atrium to the ventricle) generally fails to depolarize the whole ventricle – as the source – sink relationship is far more powerful in the conduction system bringing down the sinus impulse rather than the measly conduction coming via the AP

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